Cardiac ICAM-1 mediates leukocyte-dependent decreased ventricular contractility in endotoxemic mice☆
| Autor: | Anna Meredith, John H. Boyd, Yingjing Wang, Ehsan Y. Davani, Gurpreet K. Singhera, Delbert R. Dorscheid, Edmond Chau, Keith R. Walley |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Lipopolysaccharides
medicine.medical_specialty Lipopolysaccharide Physiology Ratón Gene Expression Inflammation Biology Contractility Leukocyte Count Mice Ventricular Dysfunction Left chemistry.chemical_compound In vivo Sepsis Physiology (medical) Internal medicine Extracellular fluid Leukocytes medicine Animals Cyclophosphamide Mice Knockout ICAM-1 Myocardium Fibrinogen Extracellular Fluid Intercellular Adhesion Molecule-1 Mice Inbred C57BL Endocrinology chemistry Circulatory system medicine.symptom Cardiology and Cardiovascular Medicine Signal Transduction |
| Zdroj: | Cardiovascular Research. 72:134-142 |
| ISSN: | 0008-6363 |
| DOI: | 10.1016/j.cardiores.2006.06.029 |
| Popis: | Objective: Binding of ICAM-1 expressed on cardiomyocytes decreases cardiomyocyte contractility in vitro by altering the intracellular Ca2+ transient. We tested the hypothesis that signaling via ICAM-1 contributes to decreased left ventricular contractility in an in vivo model of systemic inflammation. Methods: C57B6 wild-type mice and ICAM-1 knock-out mice were treated with intraperitoneal lipopolysaccharide (LPS) then left ventricular contractility was measured 6 h later using a volume-conductance micromanometer catheter. We repeated this experiment in chimeric mice lacking ICAM-1 expression in bone marrow-derived cells (M−) and/or lacking ICAM-1 expression in the heart and other tissues (H−). Results: In C57B6 wild-type mice LPS injection significantly increased cardiac ICAM-1 expression and decreased in vivo measures of left ventricular contractility (end-systolic elastance, Ees decreased 58±4%, p |
| Databáze: | OpenAIRE |
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